Copy number changes of CRISP3 in oral squamous cell carcinoma

Ko, Wen Chang; Sugahara, Kazuyuki; Sakuma, Takumi; Yen, Ching Yu; Liu, Shyun Yeu; Liaw, Gwo An; Shibahara, Takahiko

doi:10.3892/ol.2011.418

Cited by 17 publications

(11 citation statements)

References 27 publications

(25 reference statements)

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“…Notably, we find that miR-433 inhibits OSCC cell invasion and migration in the present study. Previously we observed that the MMP1 and MMP9 are up-regulated in OSCC, both of which belong to the MMP family and are responsible for the degradation of extracellular matrix components to promote cell metastasis [29][30][31]. Our study verified that miR-433 significantly suppressed the protein expression of MMP1 and MMP9.…”

Section: Discussionsupporting

confidence: 90%

miR-433 inhibits oral squamous cell carcinoma (OSCC) cell growth and metastasis by targeting HDAC6

Wang

Meng

et al. 2015

Oral Oncology

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Section: Discussionsupporting

confidence: 90%

miR-433 inhibits oral squamous cell carcinoma (OSCC) cell growth and metastasis by targeting HDAC6

Wang

Meng

et al. 2015

Oral Oncology

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“…Mixed results have been reported for a few of these DEGs in other contexts. For example, high expression of the cysteine-rich secretory protein CRISP3 (down 130-fold in NuKO cells) has been found in certain subtypes of prostate cancer [ 116 ] but down-regulation has been associated with oral squamous cell carcinoma [ 117 ]. A similar pattern has been found for the JCHAIN component of IgA and IgM (down 75-fold), which is up-regulated in prostate [ 108 ] but down-regulated in colorectal cancer [ 118 ].…”

Section: Resultsmentioning

confidence: 99%

NUDT2 Disruption Elevates Diadenosine Tetraphosphate (Ap4A) and Down-Regulates Immune Response and Cancer Promotion Genes

et al. 2016

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Regulation of gene expression is one of several roles proposed for the stress-induced nucleotide diadenosine tetraphosphate (Ap4A). We have examined this directly by a comparative RNA-Seq analysis of KBM-7 chronic myelogenous leukemia cells and KBM-7 cells in which the NUDT2 Ap4A hydrolase gene had been disrupted (NuKO cells), causing a 175-fold increase in intracellular Ap4A. 6,288 differentially expressed genes were identified with P < 0.05. Of these, 980 were up-regulated and 705 down-regulated in NuKO cells with a fold-change ≥ 2. Ingenuity® Pathway Analysis (IPA®) was used to assign these genes to known canonical pathways and functional networks. Pathways associated with interferon responses, pattern recognition receptors and inflammation scored highly in the down-regulated set of genes while functions associated with MHC class II antigens were prominent among the up-regulated genes, which otherwise showed little organization into major functional gene sets. Tryptophan catabolism was also strongly down-regulated as were numerous genes known to be involved in tumor promotion in other systems, with roles in the epithelial-mesenchymal transition, proliferation, invasion and metastasis. Conversely, some pro-apoptotic genes were up-regulated. Major upstream factors predicted by IPA® for gene down-regulation included NFκB, STAT1/2, IRF3/4 and SP1 but no major factors controlling gene up-regulation were identified. Potential mechanisms for gene regulation mediated by Ap4A and/or NUDT2 disruption include binding of Ap4A to the HINT1 co-repressor, autocrine activation of purinoceptors by Ap4A, chromatin remodeling, effects of NUDT2 loss on transcript stability, and inhibition of ATP-dependent regulatory factors such as protein kinases by Ap4A. Existing evidence favors the last of these as the most probable mechanism. Regardless, our results suggest that the NUDT2 protein could be a novel cancer chemotherapeutic target, with its inhibition potentially exerting strong anti-tumor effects via multiple pathways involving metastasis, invasion, immunosuppression and apoptosis.

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“…Down-regulation of this defense molecule in our results indicate that the inactivation of CRISP3 can be an early event able to anticipate the occurrence of cutaneous lesions. Down-regulation of CRISP3 was also detected in Squamous Cell Carcinoma skin cancer [37].…”

Section: Discussionmentioning

confidence: 99%

Investigation of serum proteome homeostasis during radiation therapy by a quantitative proteomics approach

et al. 2019

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The purpose of the present study is to analyze the serum proteome of patients receiving Radiation Therapy (RT) at different stages of their treatment to discovery candidate biomarkers of the radiation-induced skin lesions and the molecular pathways underlying the radiation signatures. Six stages of RT treatment were monitored from patients treated because of brain cancer: before starting the treatment, during the treatment (four time points), and at 4 weeks from the last RT dose. Serum samples were analyzed by a proteomics approach based on the Data Independent Acquisition (DIA) mass spectrometry (MS). RT induced clear changes in the expression levels of 36 serum proteins. Among these, 25 proteins were down- or up-regulated significantly before the emergence of skin lesions. Some of these were still deregulated after the completion of the treatment. Few days before the appearance of the skin lesions, the levels of some proteins involved in the wound healing processes were down-regulated. The pathway analysis indicated that after partial body irradiation, the expression levels of proteins functionally involved in the acute inflammatory and immune response, lipoprotein process and blood coagulation, were deregulated.

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Copy number changes of CRISP3 in oral squamous cell carcinoma

Cited by 17 publications

References 27 publications

miR-433 inhibits oral squamous cell carcinoma (OSCC) cell growth and metastasis by targeting HDAC6

miR-433 inhibits oral squamous cell carcinoma (OSCC) cell growth and metastasis by targeting HDAC6

NUDT2 Disruption Elevates Diadenosine Tetraphosphate (Ap4A) and Down-Regulates Immune Response and Cancer Promotion Genes

Investigation of serum proteome homeostasis during radiation therapy by a quantitative proteomics approach

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